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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Thursday, 2014 April 10
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results

Items 1 - 5 of 5

1.	Nature. 2014 Mar 20;507(7492):273-4. How to get ahead. [No authors listed]
	PMID: 24654276 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Mar 20;507(7492):294-5. doi: 10.1038/507294a. Technology: The $1,000 genome. Hayden EC.
	PMID: 24646979 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 Feb 28;343(6174):956. doi: 10.1126/science.343.6174.956. Science and politics. Science misused to justify Ugandan antigay law. Balter M.
	PMID: 24578555 [PubMed - indexed for MEDLINE]
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4.	Nature. 2014 Mar 20;507(7492):366-70. doi: 10.1038/nature12979. Epub 2014 Feb 23. IL-35-producing B cells are critical regulators of immunity during autoimmune and infectious diseases. Shen P1, Roch T2, Lampropoulou V3, O'Connor RA4, Stervbo U3, Hilgenberg E3, Ries S3, Dang VD3, Jaimes Y3, Daridon C5, Li R6, Jouneau L7, Boudinot P7, Wilantri S3, Sakwa I3, Miyazaki Y6, Leech MD4, McPherson RC4, Wirtz S8, Neurath M8, Hoehlig K3, Meinl E9, Grützkau A3, Grün JR3, Horn K3, Kühl AA10, Dörner T5, Bar-Or A6, Kaufmann SH11, Anderton SM4, Fillatreau S3. Author information: 11] Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany [2]. 21] Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany [2] Institute of Biomaterial Science, Helmholtz-Zentrum Geesthacht, Centre for Materials and Coastal Research, Kantstraße 55, 14513 Teltow, Germany. [3]. 3Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany. 4University of Edinburgh, Centre for Inflammation Research and Centre for Multiple Sclerosis Research, Queen's Medical Research Institute, Edinburgh EH16 4TJ, UK. 51] Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany [2] Charité Universitätsmedizin Berlin, CC12, Department of Medicine/Rheumatology and Clinical Immunology, 10117 Berlin, Germany. 6Neuroimmunology Unit, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec H3A2B4, Canada. 7Virologie et Immunologie Moléculaires, INRA, 78352 Jouy-en-Josas, France. 8Medical Clinic 1, Kussmaul Campus for Medical Research, University of Erlangen-Nürnberg, 91054 Erlangen, Germany. 9Institut für Klinische Neuroimmunologie Klinikum der Ludwig-Maximilians-Universität München, 81377 München, Germany. 10Immunpathologie, Research Center ImmunoSciences, 12203 Berlin, Germany. 11Max Planck Institute of Infection Biology, Department of Immunology, Charitéplatz 1, 10117 Berlin, Germany. Abstract B lymphocytes have critical roles as positive and negative regulators of immunity. Their inhibitory function has been associated primarily with interleukin 10 (IL-10) because B-cell-derived IL-10 can protect against autoimmune disease and increase susceptibility to pathogens. Here we identify IL-35-producing B cells as key players in the negative regulation of immunity. Mice in which only B cells did not express IL-35 lost their ability to recover from the T-cell-mediated demyelinating autoimmune disease experimental autoimmune encephalomyelitis (EAE). In contrast, these mice displayed a markedly improved resistance to infection with the intracellular bacterial pathogen Salmonella enterica serovar Typhimurium as shown by their superior containment of the bacterial growth and their prolonged survival after primary infection, and upon secondary challenge, compared to control mice. The increased immunity found in mice lacking IL-35 production by B cells was associated with a higher activation of macrophages and inflammatory T cells, as well as an increased function of B cells as antigen-presenting cells (APCs). During Salmonella infection, IL-35- and IL-10-producing B cells corresponded to two largely distinct sets of surface-IgM(+)CD138(hi)TACI(+)CXCR4(+)CD1d(int)Tim1(int) plasma cells expressing the transcription factor Blimp1 (also known as Prdm1). During EAE, CD138(+) plasma cells were also the main source of B-cell-derived IL-35 and IL-10. Collectively, our data show the importance of IL-35-producing B cells in regulation of immunity and highlight IL-35 production by B cells as a potential therapeutic target for autoimmune and infectious diseases. This study reveals the central role of activated B cells, particularly plasma cells, and their production of cytokines in the regulation of immune responses in health and disease.
	PMID: 24572363 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 Mar 20;507(7492):354-7. doi: 10.1038/nature12961. Epub 2014 Jan 29. The genomic landscape of Neanderthal ancestry in present-day humans. Sankararaman S1, Mallick S1, Dannemann M2, Prüfer K2, Kelso J2, Pääbo S2, Patterson N1, Reich D3. Author information: 11] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. 2Max Planck Institute for Evolutionary Anthropology, Leipzig 04103, Germany. 31] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA [3] Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. Abstract Genomic studies have shown that Neanderthals interbred with modern humans, and that non-Africans today are the products of this mixture. The antiquity of Neanderthal gene flow into modern humans means that genomic regions that derive from Neanderthals in any one human today are usually less than a hundred kilobases in size. However, Neanderthal haplotypes are also distinctive enough that several studies have been able to detect Neanderthal ancestry at specific loci. We systematically infer Neanderthal haplotypes in the genomes of 1,004 present-day humans. Regions that harbour a high frequency of Neanderthal alleles are enriched for genes affecting keratin filaments, suggesting that Neanderthal alleles may have helped modern humans to adapt to non-African environments. We identify multiple Neanderthal-derived alleles that confer risk for disease, suggesting that Neanderthal alleles continue to shape human biology. An unexpected finding is that regions with reduced Neanderthal ancestry are enriched in genes, implying selection to remove genetic material derived from Neanderthals. Genes that are more highly expressed in testes than in any other tissue are especially reduced in Neanderthal ancestry, and there is an approximately fivefold reduction of Neanderthal ancestry on the X chromosome, which is known from studies of diverse species to be especially dense in male hybrid sterility genes. These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.
	PMID: 24476815 [PubMed - indexed for MEDLINE]
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